Glucose Intake and Utilization in Pre-Diabetes and Diabetes

Implications for Cardiovascular Disease

Ronald Ross Watson, Betsy Dokken

• Publisher: Academic Press
• Year: 2014
• Print ISBN: 9780128000939
• eBook ISBN: 9780128005798
• Topic: Tecnología e ingeniería
• Subtopic: Endocrinología y metabolismo

This important reference, edited by Ronald Ross Watson and Betsy Dokken, collects the research needed to make the distinct connection between pre-diabetes, diabetes, and cardiovascular disease. Glucose Intake and Utilization in Pre-Diabetes and Diabetes: Implications for Cardiovascular Disease explains the mechanisms of progression from pre-diabetes to diabetes to cardiovascular disease. Since pre-diabetes and diabetes are important cardiovascular disease risk factors, and impaired glucose metabolism among cardiac patients is extremely prevalent, the importance of reviewing pre-diabetes and its involvement in CVD complications is vital as one applies food and glycemic control to slow progress to diabetes and heart disease. The book further focuses on glucose intake and utilization in diabetes, including coverage of diabetes in the development and pathology of cardiovascular disease, risks and epidemiology of cardiovascular problems promoted by diabetes, macrovascular effects and their safety in therapy of diabetics, beta cell biology and therapy of diabetes, and nutrition to modulate diabetes. - Offers a complete review of cardiac health problems occurring with significant frequency in patients relative to their ability to regulate glucose - Presents coverage of the role of glucose utilization, development of pre-diabetes and the ultimate development of various cardiovascular diseases - Provides thorough dietary, nutrition, complementary and alternative botanical therapies for pre-diabetes and diabetes to halt the progression to cardiovascular disease

Part I

Pre-Diabetes in Health and Disease: Prevention and Treatment

Outline

Section 1 Modulation of Pre-Diabetes and Altered Glucose Metabolism: Pathophysiology, Drugs, Genetics, Epigenetics, and Nutrition

Section 2 Nutrition and Food to Modulate Pre-Diabetes and Resulting Cardiac Disease

Section 1

Modulation of Pre-Diabetes and Altered Glucose Metabolism: Pathophysiology, Drugs, Genetics, Epigenetics, and Nutrition

Outline

Section 1A Background on pre-diabetes and its management

Section 1B Physiological modulators of pre-diabetes and cardiovascular disease development

Section 1A

Background on pre-diabetes and its management

Outline

Chapter 1 Early Origins of Health and Disease

Chapter 2 Diabetes and Obesity: The Impact of Their Coincidence on Health and Life

Chapter 3 Diabetes: A New Horizon and Approach to Management

Chapter 4 Psychosocial Factors Associated with Diabetes Self-Management

Chapter 5 The Relationship Between the Organization of Services for the Treatment of Type 2 Diabetes and the Risk of Long-Term Complications

Chapter 6 Effects of Bariatric Surgery on Comorbid Conditions Associated with Morbid Obesity

Chapter 7 Dietary Management of Pre-Diabetes and Type 2 Diabetes

Chapter 1

Early Origins of Health and Disease

C. Yzydorczyk, PhD¹, D. Mitanchez, MD-PhD², F. Boubred, MD-PhD³ and U. Simeoni, MD¹, ¹Division of Pediatrics & DOHaD Laboratory, CHUV University Hospital and UNIL, Lausanne, Switzerland, ²Division of Neonatology, Department of Perinatology, Armand Trousseau Hospital, 75012 Paris & Sorbonne Universités UPMC University Paris 06, Paris, France, ³Department of Neonatology, University Hospital, Marseille, France

In the 1980s, David Barker and his colleagues proposed that the major causes of cardiovascular mortality in industrialized countries may have their roots in early development. They notably observed an association between birth weight and coronary heart disease mortality rates later in life. Further epidemiological, clinical, and animal experimental studies have suggested that the time period that extends from conception through pregnancy to early infancy, also mentioned as the first 1000 days, is a critical window for the programming of lifelong health or disease. During this period, environmental stimuli potentially lead to physiological malprogramming determining final health outcomes. We review here how the early exposure to factors such as maternal undernutrition, glucocorticoids, placental insufficiency, maternal diabetes/obesity, preterm birth, oxidative stress, and epigenetic modifications can set the scene for later hypertension, obesity, and type 2 diabetes, features of the metabolic syndrome and other noncommunicable diseases.

Keywords

Fetal programming; developmental origins of health and disease; low birth weight; premature birth; noncommunicable diseases; hypertension; obesity; type 2 diabetes; metabolic syndrome

Chapter Outline

Introduction 5

Developmental Programming of MS (CVD): Human Data 6

Excess Nutrients During Fetal Growth and Long-Term Consequences 6

Mechanisms Underlying Fetal Overgrowth 6

Effects of Maternal Gestational Weight Gain 6

Consequences of Being Large at Birth 6

Consequences of Exposure to Maternal Diabetes or Obesity In Utero 7

Undernutrition During Pregnancy as a Cause of MS and CVD 8

The Consequences of Being Small at Birth 8

The Thrifty Phenotype Hypothesis 8

Maternal Caloric Restriction: the Dutch Famine 8

The Consequences of Preterm Birth 8

Effects of Postnatal Nutrition and Catch-Up Growth 9

Developmental Programming of MS (CVD): Animal Models 10

Nutritional Modifications 10

Proteins and Caloric Restriction 10

Carbohydrates 11

High-Fat Diet 11

Neonatal Overnutrition and Catch-Up Growth 11

Animal Models of Human Type 1 and 2 Diabetes 11

Animal Models of T1D 11

Animal Models of T2D 12

Animal Model of Gestational Diabetes 12

Uteroplacental Insufficiency 12

Glucocorticoids Exposure 12

Mechanisms 13

Oxidative Stress 13

Epigenetic Regulation 13

DNA Methylation 13

Histone Modifications 14

Non-coding RNAs 14

Conclusion 15

References 15

Introduction

Cardiovascular diseases (CVD) and type 2 diabetes (T2D) are usually considered diseases of adult lifestyle. Smoking, high-energy and high-fat diets, and a lack of physical exercise, which lead to overweight, hypertension (HT), dyslipidemia, and impaired glucose regulation, are risk factors for both conditions. However, there is no doubt now that adult lifestyle is not the whole story. Since the 1980s, there is increasing evidence that the roots of these adult diseases may be triggered very early in life. The Developmental Origins of Health and Disease (DOHaD) hypothesis was originally put forward by David Barker and colleagues in Southampton in the United Kingdom. In the 1980s, they observed that low birth weight (LBW), an indirect clinical marker of inappropriate intrauterine development, was inversely correlated with the risk of HT in adult life and cardiovascular mortality in a large cohort of men and women born in Hertfordshire (UK) [1]. Thereafter, this association has been observed many times by epidemiological studies in different countries and populations all over the world [2–5]. LBW as a consequence of intrauterine growth restriction (IUGR) or as a consequence of preterm birth could be responsible for CVD later in life. Excessive weight at birth also exposes the child to later metabolic disorders and CVD in adults. Furthermore, the growth of children during early life could also have an important role in the mortality from CVD.

Epidemiologic studies suggested the existence of a critical time window, from conception throughout pregnancy to early infancy, that is sensitive to long-lasting effects of environmental perturbations and therefore could potentially lead to physiological malprogramming determining final health outcomes. An exposition to certain factors during this vulnerability period, such as maternal undernutrition, glucocorticoids, placental insufficiency, maternal diabetes and obesity, and stress can set the scene for later HT, obesity, and T2D disorders, features of the metabolic syndrome (MS), and other chronic, noncommunicable diseases. The mechanisms by which exposure to altered intrauterine milieu or unsuitable early neonatal nutrition increases these risks are not fully understood. The contribution of animal models in the understanding of the mechanisms has been very important in the last years. Therefore, animal studies are critical for understanding the physiopathology of the developmental origins of adult diseases. Marked advances were also made in the last decade in deciphering the molecular mechanisms, particularly how external factors (nutritional or others) can impact the regulation and the function of genes without alteration of the genetic code.

Developmental Programming of MS (CVD): Human Data

Excess Nutrients During Fetal Growth and Long-Term Consequences

The two main conditions during pregnancy that expose the fetus to excess of nutrients are maternal diabetes and obesity. Gestational diabetes mellitus (GDM) exposes the fetus to future diseases such as obesity, HT, renal diseases, and diabetes. Maternal obesity is also tightly linked with GDM or pre-existing T2D. The risk of GDM is 2.14-fold higher in overweight pregnant women, 3.56-fold higher in obese pregnant women, and 8.56-fold higher in severely obese pregnant women compared with pregnant women with normal weight [6].

Mechanisms Underlying Fetal Overgrowth

These two maternal conditions expose the fetus to overnutrition and subsequent overgrowth and macrosomia. The mechanisms of the impact of maternal diabetes and obesity on fetal and neonatal physiology are still incompletely understood. The Pedersen’s hypothesis, formulated more than 50 years ago, suggested that fetal overgrowth was related to increased transplacental transfer of maternal glucose, stimulating the release of insulin by the fetal beta-cells. Because insulin is the fetal growth factor, subsequent macrosomia occurs [7]. Indeed, different studies have characterized the link between maternal glycemia and neonatal macrosomia or fat mass [8]. Other inter-related mechanisms play a role in the modification of fetal nutrition and metabolism and may have an impact on the long-term outcome. In GDM, apart from hyperglycemia, maternal metabolic environment is characterized by insulin resistance (IR) and inflammation [9]. Both conditions increase placental availability of nutrients to the fetus, not only glucose but also amino acids and free fatty acids, and influence fetal growth. IR facilitates maternal hypertriglyceridemia that enhances substrate availability to the fetus. Other mechanisms influence nutrient supply to the fetus. The placental transcriptome has been shown to be a target of the altered environment of diabetic pregnancy. For example, genes for lipids transport have been shown to be up-regulated in the placenta of women with GDM, as are genes for inflammatory pathways [10,11]. Altogether, such alterations directly or indirectly change the availability of substrates, other than glucose, to the fetus either by increasing their source or by modifying the materno–fetal interface. Additionally, placental epigenetic...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Dedication
• List of Contributors
• Preface
• About the Editors
• Acknowledgments
• Part I: Pre-Diabetes in Health and Disease: Prevention and Treatment
• Part II: Diabetes
• Index